Allergic rhinitis (e.g., hayfever) and bronchial asthma can result from the inhalation of specific antigenic materials (allergens) by susceptible individuals who respond with Immunoglobulin E (IgE)-mediated reactions. The interaction of the allergen with the IgE molecule, on the surface of a mast cell, leads to the release of a variety of bio-chemical mediators presumed to be responsible for symptoms such as vasodilation, edema, increased mucus secretion, cellular recruitment and increased capillary permeability. In addition to histamine, other mediators, such as the sulfidopeptide leukotrienes LTC.sub.4 and LTD.sub.4, are likely to be involved in the manifestation of many of these symptoms.
Drugs which are useful in the treatment of the above-mentioned allergic responses are believed to exert their effects by inhibiting mast cell mediator release, either by blocking the effects of these mediators on their targer cell or by relaxing airway smooth muscle. Compounds that either inhibit LTC.sub.4 induced contractions of the guinea pig ileum, inhibit edema in the rat anaphalaxis test, or inhibit the wheal reaction in the rat alergic mediator induced thermal vascular permeability test, are expected to be useful in the treatment of bronchial asthma and allergic rhinitis.